MiR-33a and statins collaboratively reduce the proliferative capacity of prostate cancer cells

Authors : Ömer Faruk Karataş, Michael ITTMANN

Pages : 266-274

Doi:10.18621/eurj.380619

View : 13 | Download : 6

Publication Date : 2018-10-04

Article Type : Research Paper

Abstract :Objectives: Prostate cancer insert ignore into journalissuearticles values(PCa); is one of the leading causes of cancer deaths among men in the developed countries. Accumulating data suggests a high-cholesterol Western diet as an important risk factor for PCa. Besides,significant evidencesassociate increased serum cholesterol levels with PCa development and progression.In this study, we aimed at investigating the collaborative roles of cholesterol analogs, cholesterol-lowering drugs, and miR-33a, which is an important microRNA involved in regulation of cholesterol metabolism,on the cellular phenotypes associated with PCa progression. Methods: We evaluated the effects of low-density lipoprotein insert ignore into journalissuearticles values(LDL); cholesterol, 25-hydroxycholesterol insert ignore into journalissuearticles values(25-HC);, mevastatin and simvastatin on their ownand together with miR-33a on the proliferation, invasion and anchorage independent growthcapacity of PCa cells using Cell Counting Kit-8, Matrigel invasion, and soft agar assays, respectively. Results: We show that cholesterol analogs significantly promoted proliferative, invasive, and clonogenic potential of PCa cells, while cholesterol loweringstatins demonstrated opposite effects. Moreover, LDL and 25-HC reversed the tumor suppressive potential of miR-33a and statin treatment promoted the proliferation inhibitory effect of miR-33a on PCa cells. Conclusions: We demonstrated that statins inhibited the cellular phenotypes associated with PCa progression and miR-33a treatment strengthens the impacts of statins on cellular proliferation. These findings suggest that statins alone and together with miR-33a might be a useful tool for effective and successful eradication of PCa cells. 
Keywords : Prostate cancer, microRNA, miR 33a, cholesterol, sttatins